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PubMed2002

Nonalcoholic fatty liver disease (NAFLD) in children.

Nonalcoholic fatty liver disease (NAFLD) is common in obese children and is a growing problem, given the increase in prevalence of obesity. NAFLD is also associated with diabetes, insulin resistance, hypercholesterolemia, and hypertriglyceridemia. Although mostly benign, some children with NAFLD develop fibrosis and cirrhosis, which necessitates close monitoring. Chronically elevated plasma liver enzyme levels is the most frequent finding. Ultrasound (US) examination allows confirmation of the diagnosis and it is useful for the follow-up. Gradual and sustained weight reduction is a management option that is worth trying initially. Other modalities of management, although interesting, await evidence as well as information on long-term benefits and effects. Sustained increase of transaminases despite weight reduction is a cause for concern and may require a liver biopsy both to assess severity of liver damage and for prognostic purposes.

Adolescent↗
PubMed1976

Dietary lysine and carnitine: relation to growth and fatty livers in rats.

Male weanling rats were fed a 72% rice diet containing no detectable carnitine and limiting in threonine and lysine. Such dietary conditions may simulate protein malnutrition in man. Under these conditions growth impairment, anemia, hypoproteinemia, and fatty liver developed. The study focused principally on the fatty liver syndrome which was corrected to varying extents depending on degrees of supplementation with carnitine, lysine, threonine, and appropriate combinations of these nutrients. Such reduction in fatty liver accumulation was accounted for principally by the lowering of triglycerides, but also in part of total cholesterol levels. All the data, which also included monitoring carnitine uptake by the tissues and measurement of plasma triglycerides, were consistent with the view that fatty liver accumulation occurs in amino acid deficient diets because (a) of an impairment in the synthesis of the lipoprotein complex mandatory for triglyceride secretion from the liver and (b) from a deficiency of carnitine needed for the intramitochondrial transport of fatty acids prerequisite for their oxidation.

Animals↗
PubMed1992

Lipoprotein metabolism in fatty liver dairy cows.

High yielding dairy cows undergo a period of energy deficit in early lactation and mobilise body reserves for milk production. During this phase lipid infiltration of the liver takes place as a result of fat mobilization and the degree of accumulation of fat in the liver depends on the level of mobilization of fatty acids from the adipose tissue. The objective of the studies reported was to characterize plasma lipoproteins in dairy cows and to determine whether differences in plasma lipoproteins existed in dairy cows with varied degrees of hepatic lipid infiltration. The physiological mechanism responsible for fatty liver is not fully understood but seems to involve a deficit in the hepatic synthesis and release of lipoproteins as shown by the depressed level and compositional modifications of plasma lipoproteins. Other results indicate a negative correlation between plasma apo B concentration and liver triglyceride content. In studies carried out on fatty liver cows the level of liver apo B mRNA was reported to be lower than in control cows. An impaired synthesis of apo B may result in its decreased availability for lipoprotein formation and in turn results in enhanced triglyceride accumulation in the liver.

Animals↗
PubMed2000

Role of hepatic lipogenesis in the susceptibility to fatty liver in the goose (Anser anser).

In response to overfeeding, the Landes goose develops a fatty liver that is twice as large as that of the Poland goose, despite similar food intake. The role of hepatic lipogenesis in the genetic susceptibility to fatty liver was assessed in male overfed geese of the two breeds. For a similar hepatic protein content, total activities of malic enzyme, glucose-6-phosphate dehydrogenase, acetyl-Coa-carboxylase and fatty acid synthase, and specific activity and mRNA level of malic enzyme were about two-fold higher in the Landes goose. In the Poland goose, the weight of the fatty liver was correlated positively with the specific activity of ME and the VLDL concentration, which was not the case in the Landes breed. These results show that: (1) hepatic lipogenesis remains very active until the end of the overfeeding period; (2) the pentose-phosphate pathway may function in birds, contrary to what is assumed usually; (3) the level of hepatic lipogenesis is a major factor in the susceptibility to hepatic steatosis in different breeds of geese; and (4) ME activity may be a limiting factor of lipid synthesis in the less susceptible Poland breed.

Acetyl-CoA Carboxylase↗
PubMed2001

Fatty liver and elevated transaminases with heterozygous apolipoprotein B deficiency.

Asymptomatic fatty liver and elevated transaminases is a common occurrence with varied etiology. Apolipoprotein (apo) B deficiency is an uncommon cause of fatty liver and elevated transaminases. The typical lipid profile low cholesterol low LDL (low density lipoprotein) suggests diagnosis of apo B deficiency and an invasive procedure like liver biopsy can be avoided in such patients.

Adult↗
PubMed1975

Factors affecting the reassociation and reactivation of the half-molecular weight nonidentical subunits of pigeon liver fatty acid synthetase.

The pigeon liver fatty acid synthetase complex (14 S) is dissociated in low ionic strength buffer containing dithiothreitol to form a half-molecular weight subunits (9 S) which are completely inactive for the synthesis of saturated fatty acids. The dithiothreitol-protected (reduced) subunits are rapidly reassociated and reactivated to form the active enzyme complex, not only by an increase in salt concentration but also by micromolar concentrations of NADP+ or NADPH. Increases in KCl or NADPH concentration result in an increase in the extent of reactivation (equilibrium) with no change in the over-all rate of the reaction or the half-life ofreactivation of the enzyme. The extent (equilibrium) of reactivation of the enzyme is the same in 0.2 M potassium phosphate buffer, pH 7.0; 0.2 M KCl in 5 mM Tris-35 mM glycine buffer, PH 8.3; and 50 muM NADP+ or NADPH in the Tris-glycine buffer. The extent and rate of reactivation of the enzyme is dependent not only on ionic strength and NADPH concentration, but also on pH and temperature. Reactivation with 0.2 M KCl is optimal between pH 7.3 and 8.5. At higher and lower pH values the rate and extent of reactivation are lowered. The rate and extent of reactivation are also decreased as the temperature is lowered below 10 degrees. At 0 degrees there is little reactivation of enzyme activity. However, in the presence of 0.2 M KCl containing 15 to 40% glycerol at 0 degrees, reactivation of the enzyme is about 50% complete. The rate of reactivation of enzyme in the presence of KCl or NADPH conforms to first order kinetics. This result suggests that the subunits first combine to form an inactive complex which is subsequently transformed to an enzymatically active complex. Evidence for the presence of inactive complex was obtained in experiments carried out in 0.2 M KCl at pH 6.0, and in 0.2 M KCl at pH 8.3, at both 6 and 3 degrees. Under these conditions the amount of complex observed upon ultracentrifugation was greater than expected from determinations of enzyme activity. The above findings suggest that ionic and hydrophobic interactions, and possibly the water structure surrounding the interacting sites, are of prime importance in reassociation and reactivation of enzyme. In addition, NADP+ and NADPH have very specific effects in bringing about reassociation and in maintaining the structural integrity of the multienzyme complex.

Animals↗
PubMed1983

Ultrasonographical diagnosis of fatty liver: significance of the liver-kidney contrast.

In order to investigate the reliability of ultrasonography in the diagnosis of fatty liver, retrospective evaluation was made of abdominal echograms in 45 patients with various diffuse liver diseases who underwent liver biopsy within 2 weeks after the ultrasound study. Instead of the well-recognized but subjective diagnostic criterion, i.e. the bright liver pattern, liver-kidney contrast is proposed as a new criterion. The liver-kidney contrast is based on the brightness of the liver in comparison to the renal parenchyma where fatty change seldom occurs. Combination of this liver-kidney contrast with two other well-known ultrasonographical findings of fatty liver, vascular blurring and deep attenuation, enables us to grade fatty change semiquantitatively. When fatty change of over 30% in the hepatic lobule was adopted as the definition of fatty liver, the satisfaction of both liver-kidney contrast and vascular blurring presented an ultrasound diagnostic criterion for fatty liver, with sensitivity of 83%, specificity of 100%, and an accuracy of 96%.

Abdominal Muscles↗
PubMed2007

The influence of pharmacogenetics on fatty liver disease in the wistar and kyoto rats: a combined transcriptomic and metabonomic study.

Although fatty liver disease is caused by a number of toxicological insults and the metabolic syndrome, the exact mechanisms by which many of these pathophysiological stimulii induce fatty liver are unknown. The rapid and profound steatosis caused by orotic acid, resulting from an impairment in the production of ApoB, has been investigated in the Wistar strain rat using a combined transcriptomic and metabonomic/metabolomic approach. Analysis of liver tissue from rats exposed to orotic acid for 1, 3, and 14 days was performed by DNA microarrays and high resolution 1H NMR spectroscopy based metabonomics of both tissue extracts and intact tissue (n = 3). Data were analyzed using a combination of ANOVA and principal components analysis, used as a data reduction tool to visualize the most perturbed transcripts and metabolites. Orotic acid produced a profound 8-fold increase in total lipids, and in particular increases in resonances associated with polyunsaturated fats (CH=CH and CH2CH=CH groups). This was accompanied by increases in the concentrations of trimethylamine-oxide (TMAO), betaine, choline, and phosphocholine, as well as a relative decrease in glucose and glycogen. At the transcriptional level, perturbations were detected in both oxidative stress and osmoregulation/pH homeostasis. However, this contrasts with a previous transcriptomic/metabolic study of fatty liver disease in a combined data set of Wistar (out-bred) and Kyoto (in-bred) strains of rats, with only 4 transcripts being found to be in common between the two analyses. This emphasizes the need to understand how strain background interacts with a given toxic lesion or genetic modification.

Animals↗
PubMed1997

Aberrant gastric venous drainage in a focal spared area of segment IV in fatty liver: demonstration with color Doppler sonography.

PURPOSE: To clarify the correlation between aberrant gastric venous drainage and a focal spared area at the posterior edge of segment IV in fatty liver by using color Doppler ultrasound (US). MATERIALS AND METHODS: Seventeen patients with fatty liver were examined with gray-scale, color Doppler, and power Doppler US. In one patient with a focal spared area, arteriography and computed tomography (CT) were performed during injection of contrast medium into the right gastric artery. RESULTS: Focal spared areas of fatty liver at segment IV were shown in five of 17 patients. In all five patients with a focal spared area, aberrant gastric venous drainage was observed with color Doppler US. Power Doppler US depicted aberrant gastric venous drainage more clearly than color Doppler US. On the other hand, no definite aberrant gastric venous drainage was seen in the 12 patients who had no focal spared area. In one patient who underwent selective arteriography of the right gastric artery and CT arteriography, aberrant gastric venous drainage into segment IV was directly demonstrated. CONCLUSION: Focal spared areas at segment IV in fatty liver correlate strongly with aberrant gastric venous drainage. Noninvasive imaging methods such as color and power Doppler US are useful for depicting these aberrant drainage veins.

Adult↗
PubMed2003

Contribution of hepatic de novo lipogenesis and reesterification of plasma non esterified fatty acids to plasma triglyceride synthesis during non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is frequently observed in insulin-resistant subjects and can lead to liver fibrosis and cirrhosis. The abnormalities of lipid metabolism behind this development of excess hepatic TG stores are poorly understood. METHODS: To clarify these mechanisms we measured triglyceride secretion rate and the contributions of hepatic lipogenesis and reesterification of non-esterified fatty acids (NEFA) to this secretion in healthy subjects and in patients with clear evidence of NAFLD. All subjects were studied in the post-absorptive state. Hepatic lipogenesis was measured with deuterated water. NEFA turnover rate, triglyceride secretion rate and the contribution of NEFA reesterification to this secretion were determined with [1-(13)C] palmitate infusion. RESULTS: NAFLD patients had higher NEFA concentrations (p<0.05) but normal NEFA turnover rates (5.23 +/- 0.80 vs 5.91 +/- 0.97 micromol.kg(-1).min(-1) in control subjects, ns). Despite a trend for higher plasma triglyceride levels in patients (p<0.10), triglyceride turnover rates were not increased (0.11 +/- 0.01 micromol.kg(-1).min(-1) in patients vs 0.14 +/- 0.01 in controls, ns). However the contribution of hepatic lipogenesis to triglyceride secretion was largely increased in patients (14.9 +/- 2.7 vs 4.6 +/- 1.1% p<0.01) while that of NEFA reesterification was reduced (25.1 +/- 2.9 vs 52.8 +/- 6.2% p<0.01). CONCLUSION: Enhanced lipogenesis appears as a major abnormality of hepatic fatty metabolism in subjects with NAFLD. Therapeutic measures aimed at decreasing hepatic lipogenesis would therefore be the most appropriate in order to reduce hepatic TG synthesis and content in such patients.

Adult↗
PubMed1995

Focal sparing of segment IV in fatty livers shown by sonography and CT: correlation with aberrant gastric venous drainage.

OBJECTIVE: One of the most common sites of focal sparing in fatty livers (focal spared area) shown by sonography or CT is the posterior edge of segment IV. The differentiation of such a focal spared area from tumor has been a diagnostic challenge. The purpose of this study was to determine if a correlation exists between the focal spared area at the posterior edge of segment IV in fatty liver and the decrease of portal perfusion from the main portal vein due to aberrant gastric venous drainage directed into segment IV. SUBJECTS AND METHODS: Seventeen patients with fatty liver diagnosed on the basis of sonographic and CT findings who had hepatic arteriography and/or CT during arterial portography (CTAP) were included in the study. Seven patients had a focal spared area more than 2 cm in the longest diameter at the posterior edge of segment IV, and 10 patients did not have a focal spared area. The frequency of aberrant gastric venous drainage shown by arteriography (17 patients) and/or by CTAP (15 patients) was compared in the two groups of patients. RESULTS: Hepatic arteriography showed aberrant gastric venous drainage in all patients who had a spared area, and CTAP showed a portal perfusion defect at the posterior edge of segment IV in all five patients with a focal spared area who underwent CTAP. On the other hand, no definite aberrant gastric venous drainage and portal perfusion defect were seen in any patient without a spared area. The difference in the frequency of aberrant gastric venous drainage between the two groups of patients was statistically significant (chi-square test, p < .0001). CONCLUSION: Our results show that a strong correlation exists between the focal spared area at the posterior edge of segment IV in fatty liver and aberrant gastric venous drainage directed to segment IV. Focally decreased blood flow from the main portal vein associated with aberrant gastric venous drainage is a likely cause of the focal spared area. This fact is important for the differential diagnosis of hepatic tumors.

Adult↗
PubMed2006

[Clinical study of treatment nonalcoholic fatty liver with qianggan capsule].

OBJECTIVE: To investigate the therapeutic effect of Qianggan capsule on the treatment of nonalcoholic fatty liver. METHODS: One hundred and twenty-two patients of nonalcoholic fatty liver were randomly divided into two groups, 64 patients in the treated group were treated by Qianggan capsule, 5 granule every time, twice per day and the 58 patients in control group were treated by tiopronin, 0. 2 gram every time, third per day with a therapeutic course of 3 months. RESULT: Serum levels of ALT and gamma-GT were decreased significantly after the treatment of Qianggan capsule (P <0.05). However, TG levels seemed decreased but have not significant difference after the treatment of Qianggan capsule. The serum level of ALT in control group decreased markedly after treatment (P < 0.05), but no obvious change was seen in gamma-GT and TG in control group after treatment. The total effective rate in the treated group was higher than those in the control group (79.69% vs 62.07%, P < 0.05). CONCLUSION: Qianggan capsule is an effective recipe in treating nonalcoholic fatty liver.

Adult↗
PubMed2006

Non-invasive markers to predict the liver fibrosis in non-alcoholic fatty liver disease.

BACKGROUND/AIM: The aim of this study was to find a non-invasive marker, which could predict liver fibrosis without the need of liver biopsy in non-alcoholic steatohepatitis (NASH). PATIENTS/METHODS: Fifty patients were included. All patients had one or more conditions that characterize the metabolic syndrome and histological proven NASH. Hyaluronic acid (HA), leptin (LT) and laminin (LN) were determined from serum withdrawn at the day of biopsy. RESULTS: Patients were divided into two groups according to the histological findings. The first group consisted of 23 patients with NASH and fibrosis and the second group had 27 patients with NASH, ballooned cells, without fibrosis. Subjects with NASH and fibrosis had statistically significantly higher HA and LN than those with NASH without fibrosis, P<0.001, respectively. In contrast, there was no statistically significant difference between the levels of serum LT in the two groups. The stage of liver fibrosis in the 23 patients of group 1 was related only to the values of hyaluronic acid (P<0.001) and not to the ones of LT and LN. CONCLUSION: Measurement of hyaluronic acid could be a predictive factor of the presence and stage of liver fibrosis in NASH. LN could be used to diagnose liver fibrosis but has no value in staging.

Adult↗
PubMed2004

Molecular mechanisms of alcoholic fatty liver: role of sterol regulatory element-binding proteins.

Alcoholic fatty liver is the earliest and most common response of the liver to alcohol in heavy alcohol use, and it may be a precursor of more severe forms of liver injury. We and colleagues in our laboratory found that in two rat hepatoma cell lines, H4IIEC3 and McA-RH7777, ethanol markedly induced transcription of a sterol regulatory element-binding protein (SREBP)-regulated promoter through increased levels of mature SREBP-1 protein. Whereas inhibition of ethanol oxidation by 4-methylpyrazole blocked the effect, the aldehyde dehydrogenase inhibitor cyanamide enhanced the effect of ethanol in the hepatoma cells, supporting the idea that the effect is likely mediated by acetaldehyde. Consistent with these in vitro findings, consumption of a low-fat diet with ethanol by mice for 4 weeks resulted in a significant increase in the abundance of the mature (active) form of hepatic SREBP-1. Activation of SREBP-1 by ethanol feeding was associated with increased expression of lipogenic genes as well as the accumulation of triglyceride in the livers. Taken together, these findings seem to indicate that metabolism of ethanol increased hepatic lipogenesis by activating SREBP-1 and that this effect of ethanol may contribute to the development of alcoholic fatty liver. We and colleagues in our laboratory further studied the mechanisms of ethanol activation of SREBP-1 by identifying a new target of ethanol, adenosine 5'-monophosphate (AMP)-activated protein kinase. Our study results demonstrated that the effect of ethanol on SREBP-regulated promoter activation was mediated, at least in part, through inhibition of AMP-activated protein kinase. Consistent with this hypothesis, chronic ethanol feeding (4 weeks) resulted in a significantly reduced activity and protein level of AMP-activated protein kinase and increased acetyl coenzyme A carboxylase activity in the mouse livers.

Animals↗
PubMed2002

Effect of charge reversal mutations on the ligand- and membrane-binding properties of liver fatty acid-binding protein.

Liver fatty acid-binding protein (FABP) is able to bind to anionic phospholipid vesicles under conditions of low ionic strength. This binding results in the release of ligand, the fluorescent fatty acid analogue 11-dansylaminoundecanoic acid (DAUDA), with loss of fluorescence intensity (Davies, J. K., Thumser, A. E. A., and Wilton, D. C. (1999) Biochemistry 38, 16932-16940). Using a strategy of charge reversal mutagenesis, the potential role of specific cationic residues in promoting interfacial binding of FABP to anionic phospholipid vesicles has been investigated. Cationic residues chosen included those within the alpha-helical region (Lys-20, Lys-31, and Lys-33) and those that make a significant contribution to the positive surface potential of the protein (Lys-31, Lys-36, Lys-47, Lys-57, and Arg-126). Only three cationic residues make a significant contribution to interfacial binding, and these residues (Lys-31, Lys-36, and Lys-57) are all located within the ligand portal region, where the protein may be predicted to exhibit maximum disorder. The binding of tryptophan mutants, F3W, F18W, and C69W, to dioleoylphosphatidylglycerol vesicles, containing 5 mol% of the fluorescent phospholipid dansyldihexadecanoylphosphatidylethanolamine, was monitored by fluorescence resonance energy transfer (FRET). All three mutants showed enhanced dansyl fluorescence due to FRET on addition of phospholipid to protein; however, this fluorescence was considerably greater with the F3W mutant, consistent with the N-terminal region of the protein coming in close proximity to the phospholipid interface. These results were confirmed by succinimide quenching studies. Overall, the results indicate that the portal region of liver FABP and specifically Lys-31, Lys-36, and Lys-57 are involved in the interaction with the interface of anionic vesicles and that the N-terminal region of the protein undergoes a conformational change, resulting in DAUDA release.

Base Sequence↗
PubMed2004

Cognitive lifetime drinking history in nonalcoholic fatty liver disease: some cases may be alcohol related.

OBJECTIVES: We aimed to determine the prevalence of significant alcohol intake in previously diagnosed nonalcoholic fatty liver (NAFL) patients. METHODS: We measured current and total lifetime alcohol intake (TLAI) in biopsy-proven NAFL patients using the cognitive lifetime drinking history (CLDH), a computerized questionnaire. One nurse administered the CLDH without physician presence. Physicians took alcohol histories prior to any knowledge of this study. Advanced and nonadvanced fibrosis patients were tested. A single pathologist (ST) scored all biopsies (inflammation 0-6; fibrosis 0-4). RESULTS: Twenty-three patients (11 men) were studied. Thirteen had bridging fibrosis or cirrhosis. [mean age: 52.3 yr (range 28-69); mean body mass index (BMI): 37 kg/m2 (range 27-48.6)]. All but three had hyperlipidemia, diabetes, and/or hypertension. Mean TLAI was 60.2 kg (range 0.17-471.7), but three patients were above 100 kg (threshold for cirrhosis risk) at 305.5, 336.7, and 471.7. These three had inflammation/fibrosis scores of 3/3, 3/0, and 5/2, respectively. Those with >100 kg tended to have higher serum AST and inflammation score. Prior physician-obtained alcohol history determined <or=20 g/day for all patients and did not mention TLAI in any. CLDH confirmed <or=20 g/day current alcohol intake in 21 of 23 patients, but intakes were 30.2 g/day and 41.2 g/day in two. CONCLUSIONS: Some NAFL patients may have alcohol fatty liver disease instead. Routine physician interviews obtain less accurate alcohol histories compared to CLDH. The clinical significance of past alcohol intake and methods of measuring alcohol ingestion in fatty liver patients deserves further investigation.

Adult↗